ABSTRACT
Background:1 α,25-dihydroxyvitamin D3 [1,25 (OH) 2 D3],the active form of vitamin D,is reported in some studies having antifibrotic potential in liver fibrosis,however,its mechanism is not fully clarified.MicroRNAs (miRNAs) have recently been shown could regulate the proliferation and activation of hepatic stellate cells (HSCs),and are involved in the promotion or inhibition of liver fibrosis.Aims:To explore whether the inhibiting effect of 1,25 (OH) 2 D3 on activation of HSCs is by regulating miRNAs expression.Methods:Literature review and qPCR method were used to screen out the differentially expressed miRNAs between transforming growth factor-β1 (TGF-β1)-stimulated (activated) HSCs and the inactivated HSCs.Then the HSCs were co-cultured with TGF-β1 and the mimic of differentially expressed miRNA,the negative control mimic,1,25(OH)2D3 and DMSO,respectively,and the cell viability and apoptosis were determined by CCK-8 assay and flow cytometry.Results:Expression of miR-146a was down-regulated in activated HSCs (P ＜ 0.05).Compared with HSCs in DMSO group,the expression of miR-146a was significantly up-regulated in HSCs treated with 1,25 (OH) 2 D3;meanwhile,the cell viability was decreased and the apoptosis was increased (P all ＜ 0.05).In HSCs transfected with miR-146a mimic,the expression of miR-146a was up-regulated,the cell viability was decreased,and the apoptosis was increased similarly with HSCs in 1,25 (OH)2D3 group (P all ＜ 0.05).Conclusions:Regulation of miR-146a expression might be one of the important mechanisms of 1,25 (OH) 2 D3 in inhibiting TGF-β1-stimulated HSC activation and inducing apoptosis in HSCs.
ABSTRACT
Objective To analyze the various common causes of acute pancreatitis distribution and related factors.Methods 131 cases of acute pancreatitis patients from April 2007 to August 2013 were chosen.The medical records were retrospectively analyzed .Patients were recorded and analyzed in age ,gender,etiology,clinical pancreatitis type.With biliary tract disease,overeating or high-fat meal,alcoholism,hyperlipidemia,other causes such as to cause the group to 18-29 years of age(youth group),29-44 years old(middle-aged group),44-59 years old(middle-aged group),≥59 years of age(age group) for the sector for the age group,for different reasons,the AP′s gender,age and different clinical types such as distribution were analyzed .Results Biliary disease 61 cases(46.3%);overeating or high-fat meal 38 cases(29.4%);alcoholism 21 cases(16.1%);high ester hyperlipidemia 8 cases(5.9%);other three cases(2.3%).Adult group overeating or high-fat meal,alcoholism and hyperlipidemia constituent ratio were higher than other groups,but with no significant difference(Pearson χ2 =19.1,df=12,P=0.085).Clinical types in a variety of different etiology than AP was no significant difference ( Pearson χ2 =1.9, df =4, P =0.753 ). Conclusion Biliary tract disease remains a major cause of AP ,followed by overeating or a high-fat meal,alcoholism, hyperlipidemia.AP has a clear upward trend,the treatment must remove the cause,to strengthen the integrated man-agement of AP .
ABSTRACT
Objective To investigate the effects of the zinc finger protein A20 on LPS-TLR4 signaling pathways in severe acute pancreatitis(SAP) rats.Methods 24 SD rats were randomly divided into 3 groups:group A(the sham operation group),group B (the SAP group),group C (the SAP group treated with LPS).SAP model was induced by retro-injection of intraductal 5％ sodium taurocholate into the biliary-pancreatic duct as previously described.The protein expression of A20,TLR4,NF-κBp65 and p38MAPK in pancreatic tissues was evaluated by immunohistochemistry.Results The positive area of A20 in pancreatic tissues was decreased in group B and group C compared with that in group A (t =17.234,19.698,all P ＜ 0.05).On the contrary,the expression of TLR4,NF-κBp65 and p38MAPK in pancreatic tissues were up-regulated(t =15.909,20.432,16.543,18.629,22.105,19.006,all P ＜ 0.05).A20 was decreased in group C than that in group B (t =14.894,P ＜ 0.05),while TLR4、NF-κBp65 and p38MAPK were increased in group C than those in group B (t =14.047,15.582,17.070,all P ＜0.05).Conclusion The expression of A20 reduced and TLR4,NF-κBp65 and p38MAPK enhanced in the pancreas of rats with SAP,which indicated that A20 inhibited LPS-TLR4 signaling pathways which play important roles in the pathogenesis of SAP.